ArticleNature communications2022
A degradative to secretory autophagy switch mediates mitochondria clearance in the absence of the mATG8-conjugation machinery.
Article in Nature communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 78 papers.
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Who cites it
78 citing papers in PubMed, 102 citations in OpenAlex.
- Review
- Mitophagy in neuronal health and disease: from mechanisms to neurodegeneration.The Journal of clinical investigation · 2026Review
- Microglial mitochondria transfer to astrocytes via GPNMB-enriched extracellular vesicles alleviates cognitive deficits in tauopathy mice.Nature neuroscience · 2026Article
- African swine fever virus B66L drives extracellular mitochondrial release to promote systemic inflammation in mice.Nature communications · 2026Article
- Targeted degradation of aberrant Tau for the discovery of Pulsatilla chinensis in Alzheimer's disease.Chinese medicine · 2026Article
- MG132-mediated inhibition of rabies virus replication via the Nrf2/SQSTM1/PINK1/Parkin autophagy pathway.Virology journal · 2026Article
- Rethinking Mitochondria: The Extracellular Dimension.Circulation research · 2026Review
- Two Routes for Removing Unhealthy Mitochondria: Degradation and Secretion.Circulation research · 2026Review
- VAMP4/STX8 Mediate the Autophagic Secretion of Mitochondria and Promote TAMs Polarization in HNSCC.Journal of extracellular vesicles · 2026Article
- The mechanisms and functions of mitochondria-encapsulating extracellular vesicles.Science China. Life sciences · 2026Review
- Review
- Visualizing extracellular vesicles in cancer: from biogenesis to theranostic applications.Journal of nanobiotechnology · 2026Review
- Mitochondria beyond boundaries: from cellular powerhouses to intercellular messengers in health and disease.Science China. Life sciences · 2026Review
- Thonningianin A derived from Penthorum chinense Pursh alleviates cerebral ischemia/reperfusion-mediated apoptosis and pyroptosis through the activation of PINK1/Parkin-dependent mitophagy.Chinese medicine · 2026Article
- Dual-function cytokines as modulators of autophagy: reprogramming inflammatory resolution in severe COVID-19.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026Review
- Targeting the secretory autophagy-extracellular vesicle interface: fate decisions and translational opportunities.Frontiers in pharmacology · 2026Review
- The Role and Therapeutic Potential of the cGAS-STING Signaling Pathway in Alzheimer's Disease.Brain and behavior · 2025Review
- MDVs bridge metabolite signals to mitochondrial fitness.Life metabolism · 2025Article
- Molecular mechanisms of mitochondrial quality control.Translational neurodegeneration · 2025Review
- Crosstalk between mitochondrial dysfunction and benign prostatic hyperplasia: unraveling the intrinsic mechanisms.The Canadian journal of urology · 2025Review
18 more citing papers are in PubMed but not listed here.
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Authors and funding
14 authors at 3 institutions in 4 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
PINK1-Parkin mediated mitophagy, a selective form of autophagy, represents one of the most important mechanisms in mitochondrial quality control (MQC) via the clearance of damaged mitochondria. Although it is well known that the conjugation of mammalian ATG8s (mATG8s) to phosphatidylethanolamine (PE) is a key step in autophagy, its role in mitophagy remains controversial. In this study, we clarify the role of the mATG8-conjugation system in mitophagy by generating knockouts of the mATG8-conjugation machinery. Unexpectedly, we show that mitochondria could still be cleared in the absence of the mATG8-conjugation system, in a process independent of lysosomal degradation. Instead, mitochondria are cleared via extracellular release through a secretory autophagy pathway, in a process we define as Autophagic Secretion of Mitochondria (ASM). Functionally, increased ASM promotes the activation of the innate immune cGAS-STING pathway in recipient cells. Overall, this study reveals ASM as a mechanism in MQC when the cellular mATG8-conjugation machinery is dysfunctional and highlights the critical role of mATG8 lipidation in suppressing inflammatory responses.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.